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J Vaamonde

Publications and source records attributed to J Vaamonde.

At least 19 recordsLinked to original sources
PubMed2001

[Motor impairment, in patients with severe Parkinson's disease, associated with dopaminergic hyperstimulation (entacapone)].

OBJECTIVE: [corrected] Entacapone was given to try to improve the motor complications in eight patients with Parkinson's disease (PD) treated chronically with levodopa, with daily severe motor fluctuations and dyskinesias. PATIENTS AND METHODS: We introduced entacapone (200 mg added to every dose of levodopa) to 8 parkinsonian patients (mean age: 68.25 +/- 2.3; range: 68-72; mean PD duration: 10.4 +/- 2.7 years) treated with oral levodopa, plus a dopa-decarboxylase inhibitor (mean dose: 706.25 +/- 2.3 mg/day; mean period of levodopa-treatment; 9 +/- 2.3 years). Dyskinesias were present in all patients (chorea: 8 patients; "off"--dystonia: 4; byphasic dyskinesias: 3). The type and duration (time "on" and "off") of fluctuations was categorized on the "on-off" charts drawn up by the patients or their relatives, and observation by the investigators after the introduction of entacapone. One patient, with severe impairment with entacapone, was evaluated (motor response) during i.v. apomorphine infusion (40 mg, during 3 hours). RESULTS: The combination of levodopa and entacapone was associated with a net increase in "off" time in all patients (from 5.8 +/- 1.2 h to 12.4 +/- 4.4 h) without change in the URPD. In the patient studied with i.v. apomorphine, "off" periods appeared during the infusion. CONCLUSION: These findings suggest that increased daily levodopa consumption may reduce striatal responsiveness to dopaminergic stimulation in severe parkinsonian patients. These data should be considered when planning the treatment strategy of complex parkinsonian patients.

Aged↗
PubMed1994

Dystonic storms: a practical management problem.

On rare occasions, torsion dystonia can rapidly worsen and produce life-threatening symptoms. We present reports on two children who had generalized dystonia and who demonstrate the management difficulties of "dystonic storms."

Child↗
PubMed1994

Motor response to apomorphine and levodopa in asymmetric Parkinson's disease.

The motor responses of 14 patients with Parkinson's disease (six previously untreated and eight chronically receiving levodopa) with pronounced asymmetry in the severity of motor signs between the left and right sides of the body were studied. The effects of a short (60 minutes) and a long (16-22 hours) intravenous levodopa infusion as well as of subcutaneous apomorphine (1-6 mg bolus) were assessed. Four different tapping tests were used to measure motor function. For all pharmacological tests, the more affected side showed a shorter response duration, increased latency, and greater response magnitude than the less affected side. These differences were more pronounced in those patients receiving chronic levodopa treatment. As apomorphine is not dependent on dopamine storage capacity, these findings suggest that postsynaptic mechanisms play an important part in the origin of motor fluctuations in Parkinson's disease.

Apomorphine↗
PubMed1993

Reflex blepharospasm associated with bilateral basal ganglia lesion.

A patient with a bilateral striatal lesion secondary to anoxia presented reflex blepharospasm associated with parkinsonism and dystonia in the limbs. The blink reflex excitability curve was enhanced and the R-2 response prolonged as in patients with essential blepharospasm. The findings in this patient support the notion that blepharospasm may be secondary to basal ganglia dysfunction through abnormal facilitation of reticular formation neurons controlling facial nucleus motoneuron excitability.

Adolescent↗
PubMed1993

Parkinsonian syndrome in childhood after sodium valproate administration.

Among the side effects attributed to sodium valproate administration, the production of a parkinsonian syndrome is very uncommon, particularly in children. We report a 12-year-old girl with secondary epilepsy; 7 days after the initiation of valproate therapy she developed parkinsonism that disappeared completely when valproate was replaced by carbamazepine. We discuss the possible role of alterations in GABAergic neurotransmission in the extrapyramidal syndrome that developed.

Child↗
PubMed1993

Cabergoline in Parkinson's disease: long-term follow-up.

We treated 36 patients with motor fluctuations and dyskinesias on chronic levodopa therapy with cabergoline (CBG) once a day for a mean period of 14.2 +/- 5.8 months. There was a significant increase in the "on" hours and a reduction in "off-period" dystonia. Ten patients continued to show a marked improvement after 28.3 months of treatment (mean dose, 11.3 +/- 4.5 mg). In 23 patients, increased dyskinesias (daily CBG dose, 11 +/- 4.3 mg) had complicated the positive effect after 17.2 +/- 4.8 months. Three patients (daily CBG dose, 14.3 mg) were therapeutic failures, and administration of CBG was stopped. Side effects leading to CBG discontinuation were visual hallucinations (n = 5), heart failure (n = 5), and nausea and vomiting (n = 1). Plasma CBG levels, measured in seven patients taking 3, 5, or 7 mg daily (po), showed fairly stable concentrations throughout the 24 hours. We concluded that CBG is an efficient dopamine agonist that can provide continuous dopaminergic stimulation when taken orally once a day.

Adult↗
PubMed1992

Levodopa-induced dyskinesias in Parkinson's disease: clinical and pharmacological classification.

Levodopa-induced dyskinesias (LID) in Parkinson's disease (PD) may be classified into three main categories: "On" dyskinesias, diphasic dyskinesias (DD), and "off" periods. The study of 168 parkinsonian patients showed that about half (n = 84) showed one pattern of LID only. A combination of two was present in 68, and 16 had the three presentation patterns. A fairly good correlation between type of dyskinesia and presentation pattern was established. Chorea, myoclonus, and dystonic movements occurred during the "on" period. Dystonic postures, particularly affecting the feet, were mainly present in the "off" period, but a few patients had a diphasic presentation. Repetitive stereotyped movements of the lower limbs always corresponded to DD. Acute pharmacological tests using dopamine agonists (subcutaneous apomorphine 3-8 mg; intravenous lisuride 0.1-0.15 mg) and dopamine antagonists (intravenous sulpiride 200-400 mg and intravenous chlorpromazine 25 mg) were performed in 40 patients. Dopamine agonists enhanced "on" dyskinesias and markedly reduced or abolished "off" period dystonia and DD. Dopamine antagonists reduced all types of LID but usually aggravated parkinsonism. These clinical and pharmacological results indicate that LID in PD are a heterogeneous phenomenon difficult to explain on the basis of a single pathophysiological mechanism.

Aged↗
PubMed1992

Motor response to repeated dopaminergic stimulation in Parkinson's disease.

Recent studies giving subcutaneous apomorphine or intravenous levodopa boluses have not found clear evidence of behavioral hyposensitivity to repeated dopaminergic stimulation in Parkinson's disease (PD). Here we analyze that data, and review experimental findings in animal models and our previous experience with parkinsonian patients. We conclude that acute tolerance to pulsatile stimulation is likely to play a role in the pathophysiology of motor fluctuations in PD.

Animals↗
PubMed1992

Acetazolamide improves action myoclonus in Ramsay Hunt syndrome.

The myoclonus of two patients with Ramsay Hunt syndrome was only partially controlled under treatment with clonazepam, sodium valproate, primidone, and piracetam. Acetazolamide (200 mg daily) was added to these drugs, resulting in a dramatic improvement. Placebo substitution (one patient) and withdrawal of acetazolamide in the other patient resulted in marked aggravation of the myoclonus. The mechanism of action of acetazolamide in myoclonus is unknown. Acetazolamide may be an additional therapeutic possibility for patients with severe action myoclonus.

Acetazolamide↗
PubMed1992

Abnormal muscle and skin mitochondria in family with myoclonus, ataxia, and deafness (May and White syndrome).

A mother and two of her daughters had deafness and cortical reflex myoclonus; the mother also had mild truncal ataxia. Muscle and skin biopsy specimens revealed abundant ragged-red fibres and abnormal mitochondria. The son of one of the daughters had sensorineural deafness. Three other grandchildren were asymptomatic. The two daughters also had diabetes mellitus, hypertension and cardiomyopathy. Another daughter died of renal failure. The mother lost her hearing in her 70s, one daughter in her 30s, and the other daughter and the grandson in their 20s. The mother has had transient episodes (24-48 hours) of temporal disorientation, severe action myoclonus, and ataxia for about eight years. This is the first reported family with inherited deafness, myoclonus, and ataxia with mitochondrial pathology.

Adolescent↗
PubMed1992

[Motor fluctuations in Parkinson disease: risk factors].

We studied the histories of 173 patients with Parkinson's disease (1985-1987) chronically treated with levodopa + dopa decarboxylase inhibitor. Ninety four patients had daily motor fluctuations and 79 showed stable motor response. The most significant differences between fluctuating and stable patients were given by age at disease onset and duration of levodopa therapy. Patient with disease onset before 60 had a greater risk (p less than 0.001) of developing fluctuations. Delaying the initiation of levodopa treatment was not associated with a smaller incidence of fluctuations.

Adult↗